OBJECTIVEThis study was to establish an animal model to imitate facial nerves injury by explosion.

METHODSThe impact was simulated by detonator blast in the distance of 5 cm, 10 cm and 15 cm over the face of dogs under anesthesia and the edge injury of masseters were made by rifle-shot steel ball to imitate segment injury in real explosion. The dogs were killed after different time of injury and the heart, lung, brain and facial nerve were taken to observe the pathological changes in order to evaluating the wound effect in different distances.

RESULTSThe animal was injured severely in the distance of 5 cm and could not survive for a long time because of severe damage to brain, heart and lung. The dogs injured at 10 cm could survive after emergency treatment, and there was diffusing hemorrhage in edematous nerve trunk. In the distance of 15 cm, the dogs were injured slightly and, as the distance to the explosive source increased, the local wound became slighter. Under light microscope, the breakage and necrosis of facial nerve fibers could be widely observed, degenerative and necrotic neurons with infiltrating inflammatory cells could be found in the facial nerve nuclei as well.

CONCLUSIONThe dog's traumatic model established by impact wave and segment in this experiment is an appropriate animal model for the research of explosive effect on facial nerves because of its controllable and repeatable injuring conditions.

Animals ; Blast Injuries ; complications ; pathology ; Disease Models, Animal ; Dogs ; Facial Nerve Injuries ; etiology ; pathology ; Female ; Male

Blast injury has become the major life- and function-threatening injuries in recent warfares. There is increased research interest in the mental disorders caused by blast-induced traumatic brain injury (bTBI), which has been proved as one of the "signature wounds" in modern battlefield. We reviewed the recent progresses in bTBI-related researches and concluded that the new era of blast injury research has shifted from the traditional physical impairments to cognitive dysfunctional/mental disorders that are proved to be more related to the outcome of combat casualty care.
Animals ; Blast Injuries ; complications ; etiology ; Brain Injuries, Traumatic ; complications ; etiology ; Cognition Disorders ; etiology ; Humans ; Mental Disorders ; etiology ; Research

The incidence of blast injury has increased recently. As the ear is the organ most sensitive to blast overpressure, the most frequent injuries seen after blast exposure are those affecting the ear. Blast overpressure affecting the ear results in sensorineural hearing loss, which is untreatable and often associated with a decline in the quality of life. Here, we review recent cases of blast-induced hearing dysfunction. The tympanic membrane is particularly sensitive to blast pressure waves, since such waves exert forces mainly at air-tissue interfaces within the body. However, treatment of tympanic membrane perforation caused by blast exposure is more difficult than that caused by other etiologies. Sensorineural hearing dysfunction after blast exposure is caused mainly by stereociliary bundle disruption on the outer hair cells. Also, a reduction in the numbers of synaptic ribbons in the inner hair cells and spiral ganglion cells is associated with hidden hearing loss, which is strongly associated with tinnitus or hyperacusis.
Blast Injuries/complications* ; Ear/injuries* ; Hearing Loss, Conductive/etiology* ; Hearing Loss, Sensorineural/etiology* ; Humans ; Tympanic Membrane Perforation/complications*

Adolescent ; Adult ; Blast Injuries ; Cilia ; Eye Foreign Bodies ; complications ; Eyelashes ; Humans ; India ; Male ; Retinal Detachment ; etiology ; physiopathology

Adolescent ; Adult ; Blast Injuries ; complications ; Deafness ; etiology ; therapy ; Female ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Treatment Outcome ; Young Adult

PURPOSEWe once reported blast-induced traumatic brain injury (bTBI) in confined space. Here, bTBI was studied again on goats in the open air using 3.0 kg trinitrotoluene.

METHODSThe goats were placed at 2, 4, 6 and 8 m far from explosion center. Trinitrotoluene (TNT) was used as the source of the blast wave and the pressure at each distance was recorded. The systemic physiology, electroencephalogram, serum level of S-100 beta, and neuron specific enolase (NSE) were determined pre and post the exposure. Neuroanatomy and neuropathology were observed 4 h after the exposure.

RESULTSSimple blast waveforms were recorded with parameters of 702.8 kPa-0.442 ms, 148.4 kPa-2.503 ms, 73.9 kPa-3.233 ms, and 41.9 kPa-5.898 ms at 2, 4, 6 and 8 m respectively. Encephalic blast overpressure was on the first time recorded in the literature by us at 104.2 kPa-0.60 ms at 2 m, where mortality and burn rate were 44% and 44%. Gross examination showed that bTBI was mainly manifested as congestive expansion of blood vessels and subarachnoid hemorrhage, which had a total incidence of 25% and 19% in 36 goats. Microscopical observation found that the main pathohistological changes were enlarged perivascular space (21/36, 58%), small hemorrhages (9/36, 25%), vascular dilatation and congestion (8/36, 22%), and less subarachnoid hemorrhage (2/36, 6%). After explosion, serum levels of S-100b and NSE were elevated, and EEG changed into slow frequency with declined amplitude. The results indicated that severity and incidence of bTBI is related to the intensity of blast overpressure.

CONCLUSIONBlast wave can pass through the skull to directly injure brain tissue.

Animals ; Blast Injuries ; complications ; Brain ; pathology ; Brain Injuries, Traumatic ; etiology ; pathology ; Electroencephalography ; Goats ; Male ; Phosphopyruvate Hydratase ; blood ; S100 Calcium Binding Protein beta Subunit ; blood

OBJECTIVETo investigate the value of susceptibility weighted imaging(SWI)in the diagnosis of hemorrhagic foci early after blast injury and its role in the outcome prediction.

METHODSTotally 30 rabbits with blast-induced cerebral blast injury were used in this study. After routine CT/MRI and SWI scanning,quantified analysis was performed in regions of interest using post-processing technology. After dissecting the brains of the experimental rabbits,the cerebral histopathological changes were observed,and the results were compared with SWI findings.

RESULTSIn these 30 rabbits,22,102,221,and 738 hemorrhagic foci were detected by CT,T1WI,T2WI,and SWI,respectively. The number of cerebral microbleeds detected by SWI was significantly larger than those revealed by conventional T1WI and T2WI(Χ(2)=10.00,P<0.01). Furthermore,the SWI imaging displayed the punctiform(n=315,42.7%),lamellar(n=218,29.5%),slinar(n=205,27.8%)hypointense foci,with clear margin. The number of hemorrhagic foci detected by SWI was positively correlated with survival(r=-0.667,P<0.05).

CONCLUSIONSSWI remarkably increases the detection rate of hemorrhagic foci(particularly microbleeds)in rabbits with cerebral blast injury. The number of cerebral microbleeds and location of foci are closely related with the outcomes and therefore may facilitate clinical managment.

Animals ; Blast Injuries ; complications ; diagnosis ; Brain ; pathology ; Brain Injuries ; diagnosis ; etiology ; Cerebral Hemorrhage ; diagnosis ; etiology ; Female ; Image Enhancement ; Magnetic Resonance Imaging ; methods ; Male ; Prognosis ; Rabbits

BACKGROUNDSevere burn-blast combined injury is a great challenge to medical teams for its high mortality. The aim of this study was to elucidate the clinical characteristics of the injury and to present our clinical experiences on the treatment of such cases.

METHODSFive patients with severe burn-blast combined injuries were admitted to our hospital 77 hours post-injury on June 7, 2005. The burn extent ranged from 80% to 97% (89.6% +/- 7.2%) of TBSA (full-thickness burns 75% - 92% (83.4% +/- 7.3%)). All the patients were diagnosed as having blast injury and moderate or severe inhalation injury. Functions of the heart, liver, kidney, lung, pancreas and coagulation were observed. Autopsy samples of the heart, liver, and lungs were taken from the deceased. Comprehensive measures were taken during the treatment, including protection of organ dys function, use of antibiotics, early anticoagulant treatment, early closure of burn wounds, etc. All the data were analyzed statistically with t test.

RESULTSOne patient died of septic shock 23 hours after admission (four days after injury), the others survived. Dysfunction of the heart, liver, lungs, pancreas, and coagulation were found in all the patients on admission, and the functions were ameliorated after appropriate treatments.

CONCLUSIONSBurn-blast combined injury may cause multiple organ dysfunctions, especially coagulopathy. Proper judgment of patients' condition, energetic anticoagulant treatment, early closure of burn wounds, rational use of antibiotics, nutritional support, intensive insulin treatment, timely and effective support and protection of organ function are the most important contributory factors in successful treatment of burn-blast combined injuries.

Adult ; Anti-Bacterial Agents ; therapeutic use ; Blast Injuries ; complications ; physiopathology ; therapy ; Burns ; complications ; physiopathology ; therapy ; Humans ; Male ; Nutrition Therapy ; Psychotherapy ; Respiration

Accidents, Occupational ; Acetic Anhydrides ; Adult ; Blast Injuries ; complications ; therapy ; Burns, Inhalation ; etiology ; therapy ; Humans ; Lung Injury ; etiology ; therapy ; Male ; Middle Aged

OBJECTIVETo investigate the effects of three different ways of chronic caffeine administration on blast- induced memory dysfunction and to explore the underlying mechanisms.

METHODSAdult male C57BL/6 mice were used and randomly divided into five groups: control: without blast exposure, con-water: administrated with water continuously before and after blast-induced traumatic brain injury (bTBI), con-caffeine: administrated with caffeine continuously for 1 month before and after bTBI, pre-caffeine: chronically administrated with caffeine for 1 month before bTBI and withdrawal after bTBI, post-caffeine: chronically administrated with caffeine after bTBI. After being subjected to moderate intensity of blast injury, mice were recorded for learning and memory performance using Morris water maze (MWM) paradigms at 1, 4, and 8 weeks post-blast injury. Neurological deficit scoring, glutamate concentration, proinflammatory cytokines production, and neuropathological changes at 24 h, 1, 4, and 8 weeks post-bTBI were examined to evaluate the brain injury in early and prolonged stages. Adenosine A1 receptor expression was detected using qPCR.

RESULTSAll of the three ways of chronic caffeine exposure ameliorated blast-induced memory deficit, which is correlated with the neuroprotective effects against excitotoxicity, inflammation, astrogliosis and neuronal loss at different stages of injury. Continuous caffeine treatment played positive roles in both early and prolonged stages of bTBI; pre-bTBI and post-bTBI treatment of caffeine tended to exert neuroprotective effects at early and prolonged stages of bTBI respectively. Up-regulation of adenosine A1 receptor expression might contribute to the favorable effects of chronic caffeine consumption.

CONCLUSIONSince caffeinated beverages are widely consumed in both civilian and military personnel and are convenient to get, the results may provide a promising prophylactic strategy for blast-induced neurotrauma and the consequent cognitive impairment.

Animals ; Blast Injuries ; complications ; Brain Injuries, Traumatic ; complications ; Caffeine ; pharmacology ; Cerebral Cortex ; pathology ; Hippocampus ; pathology ; Male ; Memory Disorders ; etiology ; prevention & control ; Mice ; Mice, Inbred C57BL ; RNA, Messenger ; analysis ; Receptor, Adenosine A1 ; genetics